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Since right ventricular (RV) dysplasia was described in an autopsy case series of young adults with sudden cardiac death (SCD) in the early 1980s,1 researchers have sought to unravel the complex relationship between exercise and SCD in arrhythmogenic right ventricular cardiomyopathy (ARVC). Advanced cardiac imaging and genetic testing have since enriched our understanding of how pathogenic variants in an expanding array of genes manifest cardiomyopathy of either ventricle and a propensity toward ventricular arrythmia. The more inclusive term arrhythmogenic cardiomyopathy (ACM) was created to recognise the potential for left ventricular (LV), RV or biventricular involvement. However, while the initial reports of ARVC lacked the phenotyping and genotyping that are commonplace today, they did report on the close association between physical exertion and ventricular arrhythmias, as 10 of the 60 initially described patients had died during exertion.1
Subsequent studies have provided more granular definitions of athletics using metabolic equivalents (METs) and disarticulating recreational athletes from competitive ones. Exercise demonstrates a direct and dose-dependent relationship with ventricular arrythmia risk as well as with structural abnormalities and remodelling, including ventricular size, ejection fraction and risk of heart failure.2 3 Our understanding of the genetics underlying ACM lends credibility to the hypothesis that exercise precipitates arrhythmia and structural remodelling in predisposed individuals. ACM …
Contributors Both authors contributed to the conception, literature search, drafting and manuscript editing.
Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Competing interests None declared.
Provenance and peer review Commissioned; internally peer reviewed.